The Campbell model of prophage integration and excision is based on the formation of a cyclic viral genome which undergoes a site specific recombination with the host chromosome. Although this model has proven extremely useful in analyzing the lysogenic replication cycles of phages such as lambda, the model does not appear applicable to the temperate Bacillus subtilis phage Phi 105. Excision of the integrated Phi 105 prophage occurs in some unknown manner from a replicating complex of bacterial and phage DNA. The mechanism of Phi 105 integration is even less well understood. We propose to study the viral and host functions regulating the establishment and reversal of the Phi 105 lysogenic state. Our approach is based largely on the usefulness of mutant analysis as a means of dissecting regulatory pathways. Lysogenic-defective phage mutants have been isolated and are being arranged into complementation groups to identify the phage genes involved in lysogenization. Several of these mutants appear to be deletions in gene function(s) required for the maintenance of lysogeny. Another mutant forms a prophage which is not inducible by UV irradiation but is induced by recombinational events associated with DNA mediated transformtion. The mechanism of this unique mode of prophage induction will be examined. Through the use of non-inducible mutants we have demonstrated that the physiological state of transformation-competent cells can also lead to prophage derepression and we are investigating the basis for this phenomenon. BIBLIOGRAPHIC REFERENCES: Thurm, P.T. and A.J. Garro (1975). Isolation and characterization of prophage mutants of the defective Bacillus subtilis phage PBSX. J. Virol. 16:184-191. Garro, A.J., C. Sprouse and J.G. Wetmur (1976). Association of the recombination-deficient phenotype of Bacillus subtilis rec C strains with the presence of an SPO2 prophage. J. Bacteriol. 126:556-558.